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PubMed2002

[Acute papillary muscle rupture and mitral valve insufficiency after myocardial infarction. Serious condition, but potentially curable through emergency surgery].

Acute papillary muscle rupture resulting in severe mitral regurgitation is an infrequent but extremely serious mechanical complication of myocardial infarction. The immediate and severe volume overload on the pulmonary circulation may cause pulmonary edema and circulatory shock with secondary organ failure. Diagnosis is preferably based on echocardiography, and urgent mitral valve replacement is the treatment of choice. This paper describes two such patients who were successfully treated by surgery despite cardiogenic shock. In addition, it illustrates the known fact that a papillary muscle rupture may be caused by a myocardial infarct of limited size but with an unfortunate location.

Acute Disease↗

PubMed1977

Metal-film thermopiles for use with rabbit right ventricular papillary muscles.

A method of fabricating Hill-Downing type, planar thermopiles by vacuum-deposition techniques is described in detail. The present model was designed for initial heat measurements on rabbit papillary muscles as small as 1 mg blotted wt, but it is also suitable for small bundles of frog muscle fibers (30-75). The thermopile has 20 or 14 junctions, an active length of 5 or 3.5 mm, and an actual thickness of 20 micrometer. It has an effective heat capacity of about 0.3 mcal/degrees C, a heat loss coefficient of about 0.3 mcal/degrees C - s, a temperature sensitivity of 1.4 mV/degrees C (20 junctions), and an electrical resistance of 180-200 omega. Infrared-emitting diodes are used to heat the thermopile and muscle artificially for thermal time constant and conduction-delay measurements. Performance of the thermopiles is demonstrated with initial heat records from rabbit right ventricular papillary muscles and a bundle of frog semitendinosus muscle fibers. Results of preliminary experiments concerning latency for heat generation, initial rate of heat generation, and activation heat in both types of muscles are presented.

Alloys↗

PubMed1981

[Efflux of 36Cl and the distribution of chlorine in the papillary muscles of rabbits and the effect of ouabain].

The 36Cl efflux "in vivo" was measured in the rabbit papillary muscle to determine the Cl distribution in the muscle and to evaluate the effect of ouabain on this parameter. The results obtained for the 36Cl efflux are analyzed using either a two-compartment model or a model including diffusion in the extracellular space in series with one compartment. The Cl exchange with 36Cl, [Cl]i (intracellular Cl content which has participated in exchange, Cl in equilibrium with 36Cl) is computed from the exponential terms of the models. A time exposure of 40 and 80 min to the 36Cl-containing solution led to the same exchange Cl content: 20.5 and 23.9 mmol/kg cells. Addition of ouabain (10(-6) M) slightly increased the rate constant of the cellular compartment, but did not influence the [Cl]i. In the presence of ouabain (10(-6) M), there was a significant increase in the efflux component with a rapid rate constant. These results can be interpreted as follows: the Cl intracellular concentration is not affected by ouabain; thus, the increase in total Cl content induced in the papillary muscle by ouabain is located in a compartment having a very rapid exchange velocity with the extracellular medium.

Animals↗

PubMed1980

Ischemic papillary muscle necrosis in stressed newborn infants.

The recent association of transient tricuspid insufficiency in newborn infants with ischemic papillary muscle necrosis prompted a detailed retrospective clinical and histologic analysis of autopsied infants who died within seven days of birth between 1973 and 1977. Infants with congenital heart disease, erythroblastosis fetalis, and known congenital viral infections were excluded. Thirty-one of 82 infants had at least one site of ischemic myocardial necrosis: 11 had lesions only in the right ventricle, 13 had lesions only in the left ventricle, and seven had bilateral lesions. The apical region of an anterior papillary muscle was the most common site. IMN occurred more commonly in older, larger infants. Asphyxia at birth, a murmur of atrioventricular valve insufficiency, and signs of congestive heart failure correlated well with the presence of IMN, but few other perinatal events predicted its occurrence. This report suggests that IMN is a common event in stressed infants who die early in life and probably is related to episodic hypoperfusion of the myocardium.

Apgar Score↗

PubMed1990

The cellular electropharmacology of mexiletine combined with sotalol in porcine papillary muscle and Purkinje fibre. II. Effects on action potential duration and refractoriness.

Using standard microelectrode techniques, the authors compared the effects of 15 to 125 microM concentrations of mexiletine, 31 to 500 microM concentrations of sotalol and 15 to 125 microM of mexiletine combined with 125 microM sotalol, on the beat-to-beat action potential duration and refractoriness of porcine papillary muscles and Purkinje fibres stimulated by 30 beat trains at a frequency of 1 Hz. Sotalol alone prolonged action potential duration and effective refractory period without altering their ratio. Mexiletine shortened action potential duration while prolonging refractoriness. When the two drugs were combined, action potential duration was shortened to the same extent as with mexiletine alone, but refractoriness, particularly in papillary muscle, was further prolonged. These changes suggest additive inhibition of the sodium window current by both drugs. Purkinje action potential duration was longest in the first beat of the train, while in papillary muscle, this beat was shortest. Exposure to either or both drugs eliminated the prolongation of duration of the first beat of the train in Purkinje fibre. Thus, the phenomenon of restitution, which prolongs the duration of the first beat after a long diastolic interval, appears also to be related to the sodium window current.

Action Potentials↗

PubMed1984

Adenosine and prostacyclin independent electrophysiological effects of dipyridamole in guinea-pig papillary muscles and canine cardiac Purkinje fibers.

Dipyridamole was initially introduced as a coronary vasodilator. The exact mechanism of action of dipyridamole on the coronary vasculature is unknown, but proposed mechanisms of action include inhibition of adenosine uptake, increased myocardial prostacyclin production and inhibition of phosphodiesterase activity. The purpose of our study was to examine the electrophysiological effects of dipyridamole on guinea-pig papillary muscles and canine cardiac Purkinje fibers to determine whether similar mechanisms might account for the electrophysiological effects of this compound. Conventional microelectrode techniques were used to record transmembrane action potentials from either guinea-pig papillary muscles or canine cardiac Purkinje fibers. Dipyridamole produces a dose-dependent prolongation of action potential duration with a threshold concentration of approximately 5 X 10(-7) M in tissues from either species. Dipyridamole (10(-5) M) increases action potential amplitude (124 +/- 1 to 127 +/- 1 mV), increases action potential duration (119 +/- 6 to 146 +/- 5 msec) and produces hyperpolarization of the resting potential (-85 +/- 1 to -87 +/- 1 mV) in guinea-pig papillary muscles (n = 27, P less than .05). Dipyridamole (10(-5) M) increases action potential duration (276 +/- 5 to 293 +/- 5 msec) in canine cardiac Purkinje fibers (n = 21, P less than .05). The effects of dipyridamole (5 X 10(-7) M) are neither accentuated by adenosine (10(-4) M) nor attenuated by adenosine deaminase (1 U/ml) Pretreatment with indomethacin (10(-5) M) does not block these effects. Dipyridamole (10(-5) M) produces a negative chronotropic response in canine Purkinje fibers, increases mean escape intervals from 4.9 +/- 0.9 to 7.8 +/- 1.4 sec (n = 8, P less than .05) and fails to suppress slow response action potentials in 22 mM K+ depolarized tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1985

[Mitral valve replacement with preservation of whole papillary muscles and chordae tendineae].

A total of 20 patients underwent mitral valve replacement (MVR) with preservation of the papillary muscles (PM) and chordae tendineae (CT) with the object of maintaining left ventricular contractility and decreasing the risk of left ventricular rupture after surgery. The patients comprised of 8 males and 12 females whose ages ranged from 33 to 67 years. In 8 patients, the posterior leaflet was left in place and in 12, the CT to the anterior leaflet were also preserved by excision of the central portion and reattachment of the rest of the leaflet to the appropriate commissural regions. St. Jude Medical valves were exclusively employed as a substitute. Reasons for MVR were isolated MR in 12 cases, MRs in 5 and MSr in 3. There were one operative, one hospital and one late death respectively. Postoperative C.I. increased from 2.65 +/- 0.48 to 3.8 +/- 0.75 ml/min./M2 and LVEF increased from 55.1 +/- 11.4 to 63.4 +/- 13.4%. The area method showed marked improvement of segmental wall motion in anterolateral regions. Chordal shortening also disclosed improvement in long axis. Preservation of papillary muscles and chordae tendineae during MVR has been found to have a beneficial effect on postoperative left ventricular contractility.

Adult↗

PubMed2000

Frequency- and time-dependent effects of fendiline on action potentials of guinea pig papillary muscle.

The action of fendiline on cardiac electrical activity was investigated in guinea pig papillary muscle by monitoring frequency- and time-dependent changes in membrane potential, action potential (AP) configuration and conduction velocity. Isolated guinea pig papillary muscles driven at 0.1 to 3 Hz showed a concentration-dependent reduction of +Vmax, overshoot, and AP duration at -20mV (APD20) in the presence of fendiline (1-320 microM), reflecting inhibition of Na+ and L-type Ca2+ channels, respectively. No significant change in resting potential and AP duration at 90% repolarization (APD90) were observed. Inhibition of +Vmax and APD20 was more prominent at higher frequency of stimulation (2 Hz) than at lower ones (0.2 Hz), demonstrating frequency-dependent block of Na+ and Ca2+ channels including an open channel block. A good relationship between changes in +Vmax and APD20 suggested some commonality in the mechanism of inhibition of Na+ and Ca2+ channels by fendiline. Time-dependence of effects of fendiline, observed in presence of bolus dose (200 microM), showed an earlier onset of inhibition of +Vmax and APD20, particularly at higher frequencies. Missed beats and conduction block also appeared earlier in preparations driven at higher frequency. These findings suggest a frequency-dependent (and open channel) block of Na+ and Ca2+ channels by fendiline, leading to inhibition of fast and slow conduction in addition to its reported inactivated Ca2+ channel block.

Action Potentials↗

PubMed1982

Surface layer ATP-related contraction in isolated, superfused canine ventricular papillary muscle: an isotachophoretic analysis.

The relationship among contractile tension, ATP content and concentration was examined in isolated, superfused ventricular papillary muscle under normoxic (Po2 not equal to 300 mmHg) and hypoxic (Po2 not equal to 100 mmHg) conditions, using capillary isotachophoresis. The muscle preparations were exposed to each condition for 30 min, and the contractile tension was recorded with a strain gauge. Immediately after the recordings, the preparations were homogenized and the metabolites (ATP, ADP, AMP, creatine phosphate, inosine monophosphate, NAD, NADH, glucose-6-phosphate, pyruvate, and inorganic phosphate) were extracted in 50% methanol-1.25 mM EDTA solution at -20 degrees C for 4 days. The supernatant of the extract was used for the isotachophoretic analysis. Hypoxia markedly depressed ATP content and concentration in the tissue. Under conditions of normoxia, but not hypoxia, the developed tension positively correlated with the ATP content and concentration. Under normoxic conditions, the tension tended to be proportional to the estimated surface area of the preparation, while in hypoxia it tended to be inversely proportional thereto. The ATP concentration appeared to be inversely proportional to the muscle weight, thereby suggesting that the outer layer of the preparation contains more ATP than the inner. In fact, an isotachophoretic analysis of the tissue revealed significantly higher ATP concentrations in the outer layer. Our findings indicate that there is a central anoxic core in the isolated canine papillary muscle superfused with oxygenated Tyrode solution and that surface layer ATP probably plays a pivotal role in the initiation of contraction.

Adenosine Triphosphate↗

PubMedDate not supplied

Traumatic left ventricular papillary muscle rupture: the role of transesophageal echocardiography in diagnosis and surgical management.

We report a case of left ventricular posteromedial papillary muscle rupture caused by blunt chest trauma. Transesophageal echocardiography was used to establish the diagnosis and to assist with surgical repair of the mitral valve apparatus. Echocardiographic findings of the acutely ruptured papillary muscle are reviewed.

Accidents, Traffic↗

PubMed1991

Thyroid state and electrical properties of rat papillary muscle fibres.

We have studied the effects of in vivo alterations of thyroid state on the electrophysiological properties, measured in vitro, of rat papillary muscle fibres. The duration of the action potential, recorded from single cells of papillary muscle obtained from 60 day old rats, thyroidectomized at weaning, was larger than in preparations of euthyroid animals of same age. The treatment of thyroidectomized rats with T3 physiological doses restored the values of action potential duration present in euthyroid animals of same age. The data dealing with the time course of these variations indicate a late effect of thyroidectomy or T3 treatment. The hyperthyroid state, obtained by treatment of thyroidectomized rats with larger doses of T3, was associated with a significant reduction in the action potential. Action potential duration is frequency dependent. As the stimulation rate was increased from 1 to 5 Hz, this duration increased in all groups. However the difference found among the rat groups remained significant. Propranolol had virtually no effect on action potentials from fibres of euthyroid animals and those in altered thyroid state.

Action Potentials↗

PubMed1987

Force, velocity, and power changes during normal and potentiated contractions of cat papillary muscle.

The instantaneous force-velocity relations of cat papillary muscles were studied at different times in the twitch in normal and in postextrasystolic potentiated contractions. Fourteen to sixteen different loads were used to define each of the force-velocity curves. The curves were fitted by a least-squares procedure to the hyperbolic (Hill equation). The hyperbolae were extrapolated to obtain maximum velocity and isometric force and interpolated to obtain maximum power. All three of these values rose more quickly than developed force. Maximum velocity reached 77% of its peak at the earliest time studied, 20-25% of the time to peak force. Developed force achieved 22% of its final value at this time, while extrapolated isometric force and maximum power both reached 44% of their peak values. Postextrasystolic potentiation sufficient to produce a 1.5 to twofold increase in peak developed force produced less than a 20% increase in extrapolated maximum velocity. The results can be interpreted in terms of a model in which the maximum velocity of the contractile elements remains constant during the twitch. Variation in maximum velocity is attributed to a small internal load, equivalent to 6% of twitch force. Since maximum velocity is relatively constant, it does not give a good measure of changes in the force-velocity curves. By contrast, the extrapolated isometric force and maximum power are much more sensitive to changes in the force-velocity curves, and they vary in proportion to each other. The advantage of using interpolated maximum power rather than isometric force to define changes in the curves is that it can be normalized to muscle mass.

Animals↗

PubMed1988

Phorbol ester does not mimic, but antagonizes the alpha-adrenoceptor-mediated positive inotropic effect in the rabbit papillary muscle.

The phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) was used to examine the hypothesis that phosphoinositide turnover is involved in the regulation of myocardial contractility mediated by stimulation of alpha-adrenoceptors in the mammalian cardiac muscle. Exposure of the isolated rabbit papillary muscle electrically driven at a rate of 1 Hz at a temperature of 37 degrees C to TPA in concentrations of 10-1000 nmol/l for 30 min did not affect the basal force of contraction. The concentration-response curve for the positive inotropic effect of (-)-phenylephrine mediated by stimulation of alpha-adrenoceptors in the presence of (+/-)-bupranolol (100 nmol/l) was shifted to the right and downward by TPA in concentrations of 30-1000 nmol/l, while the effect of (-)-phenylephrine mediated by stimulation of beta-adrenoceptors in the presence of prazosin (100 nmol/l) was not decreased, but slightly enhanced by exposure of the muscle to relatively low concentrations of TPA (10-100 nmol/l). Incubation of the membrane fraction isolated from the rabbit ventricular muscle with TPA in vitro under the same condition as employed in the physiological experiments decreased the specific binding of [3H]prazosin but not that of [3H]CGP-12177, while the non-tumor promoting phorbol ester, alpha PDD, was ineffective. These results indicate that activation of protein kinase C by TPA does not mimic the positive inotropic effect of catecholamines mediated by activation of myocardial alpha-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1980

Dystrophic degeneration of papillary muscle and ventricular myocardium. A basis for mitral valve prolapse in Duchenne's muscular dystrophy.

The hearts of three children who died with Duchenne's progressive muscular dystrophy and features of mitral valve prolapse were examined to find if the valve disorder arose from cardiomyopathy due to the primary disease or from dystrophic changes in th mitral valve itself. Gross, histologic and ultrastructural features of mitral valve annulus, anterior and posterior leaflets, chordae tendineae, right and left ventricles, and anterior and posterior papillary muscles were compared with those of similar tissues from normal children of matched age and sex. Fibrosis and myofibrillar lysis--most extensive in posterior papillary muscle and in the posterobasal segment of the left ventricle--were the main histopathologic findings. Myofibrillar lysis was characterized by a total loss of actin and myosin myofilaments. By contrast, the mitral valve annulus, its leaflets and the origin, distribution pattern, length and thickness of chordae tendineae were entirely normal. These observations establish that mitral valve prolapse syndrome in Duchenne's dystrophy is an expression of cardiomyopathy involving papillary muscle and ventricular myocardium rather than a result of dystrophic changes in the mitral valve leaflets, annulus or chordae tendineae.

Adolescent↗

PubMed1982

[Two-dimensional echocardiographic findings of patients with papillary muscle dysfunction].

Two-dimensional echocardiographic examination was performed to investigate pathophysiological mechanism of mitral regurgitation due to papillary muscle dysfunction in 6 patients with myocardial infarction (anterior : 3, inferior: 2 and subendocardial: 1) and 13 patients with dilated cardiomyopathy. The patients were divided into 2 groups; Group I was 9 with mitral valve prolapse and Group II was 10 without mitral valve prolapse (MVP). In Group I MVP was observed in the posterior leaflet in 6 and in both leaflets in the remainder. The apical four-chamber view of all patients in Group II showed that the point of mitral valve coaptation displaced toward the apex of the left ventricle during systole and the both mitral leaflets were convexed toward the left ventricle. Follow-up observation in a patient with dilated cardiomyopathy revealed that the heart was not enlarged (CTR 50%), no murmur was heard and mild anterior mitral leaflet prolapse was observed in 1979, but, in 1981, CTR became 63%, and a grade IV systolic murmur suggesting mitral regurgitation was noted. Two-dimensional echocardiography revealed that mitral leaflets became convex toward the left ventricle and coaptation point of the mitral closure shifted to the apex of the left ventricle below the level of mitral annulus. Thus, the transition to Group II from Group I was suggested. Echocardiographic measurements revealed that left ventricular end-diastolic dimension was 71 +/- 11 mm in Group I and 74 +/- 10 mm in Group II, left ventricular end-systolic dimension was 61 +/- 11 mm in Group I and 62 +/- 11 mm in Group II, and anterio-posterior mitral ring dimension was 31 +/- 3 mm in Group I and 35 +/- 3 mm in Group II (p less than 0.05). In conclusion, it was suggested that two mechanisms of mitral regurgitation are present in papillary muscle dysfunction; 1) mitral valve prolapse and 2) shift of mitral coaptation point toward the apex of the left ventricle associated with marked dilatation of the mitral annulus.

Adult↗

PubMed1993

Mitral regurgitation from papillary muscle rupture: role of transesophageal echocardiography.

A case of a 61 year old male with lateral myocardial infarction, congestive heart failure and fever of days is presented. The exact etiology of this patient's heart failure was established with the application of transesophageal echocardiography. The transthoracic two-dimensional and Doppler echo showed a mobile echogenic density attached to the tip of the anterior mitral leaflet accompanied by moderate mitral regurgitation. Transesophageal echocardiography attributed this echogenic density to a ruptured head of the anterolateral papillary muscle, resulting in severe mitral regurgitation. Cardiac catheterization confirmed the severe mitral regurgitation and uncovered significant stenotic lesions of the coronary arteries. The resultant surgical treatment for the replacement of the mitral valve and coronary artery by-pass confirmed the rupture of the head of the anterolateral papillary muscle. It is suggested that transesophageal echocardiography is particularly capable of providing a definitive and prompt diagnosis of papillary muscle rupture.

Coronary Artery Bypass↗

PubMed1998

Mechanism of hypoxic preconditioning in guinea pig papillary muscles.

UNLABELLED: Brief ischemia or hypoxia has been found to protect the heart against subsequent long-lasting ischemia and to improve contractile dysfunction as well to reduce cell necrosis and the incidence of lethal arrhythmias. This phenomenon, termed preconditioning (PC) has been demonstrated in different species. However, little is known about PC in guinea pigs. Moreover, electrophysiological changes underlying protection have not been studied so far in conjuntion with force recovery in a setting of PC. The aim of the study was to study PC in a guinea pig papillary muscle, using recovery of contractility after long hypoxic challenge as the main end-point of protection, and to investigate concomitant electrophysiological alterations. In guinea pig papillary muscle preparations contracting isometrically (paced at 2 Hz), transmembrane action potentials (AP) and developed force (DF) were recorded by conventional microelectrode technique and a force transducer. In addition, effective refractory periods (ERP) were determined. Hypoxia was induced by superfusion with 100% N2 (pO2 < 5 kPa) and pacing at 3,3 Hz. In the control group, long hypoxia lasted for 45 min and was followed by 30 min reoxygenation. In the PC group, muscles were subjected to 5 min hypoxia followed by 10 min recovery prior to sustained hypoxia/reoxygenation. RESULTS: Long hypoxia induced a similar depression of DF in both, PC and control groups. However, a loss of contractile activity occured earlier in the PC group. AP duration and ERP decreased faster and were significantly shorter after PC. Upon reoxygenation, preconditioned muscles showed significantly better recovery of function (DF 86% of prehypoxic value vs. 36% in controls; p < 0,05). AP and ERP were completely restored in both, PC and control groups. Guinea pig papillary muscle can be preconditioned with a brief hypoxic challenge against contractile dysfunction upon long-lasting hypoxia/reoxygenation. Shortening of AP and loss of contractility occured more quickly during hypoxia and may participate in the protective effect of preconditioning. Possible mechanisms might involve facilitated opening of K(ATP)-dependent channels.

Action Potentials↗

PubMed1992

[Pathogenesis of mitral valve prolapse in patients with chronic Chagas disease: study of papillary muscle myocarditis].

PURPOSE: Studying the mitral valve in chronic Chagas' heart disease, searching a possible cause effect relationship between this condition and valve prolapse. METHODS: Seventeen hearts were surveyed from individuals exhibiting chronic chagasic cardiopathy, 11 males and 6 females, aged between 31-84 (average 54) years. The hearts came from necropsies carried out until a year before. Properly preserved samples were analyzed macro and microscopically. Fragments were excised from the mitral valve papillary muscles, anterior, lateral and posterior regions of the left ventricle, interventricular septum, free wall of right ventricle and atrium walls. RESULTS: Chronic myocarditis was found ill all the samples (mild in 6 of them, moderate in 7 and severe in 4). Also, the papillary muscles exhibited myocarditis in all of the samples, and in 15 of them the degree of severity was equal to or superior than the observed in degree other regions of the heart. CONCLUSION: The chronic chagasic cardiopathy, the papillary muscle constitute a frequent site of myocarditis. This fact must be held in mind when one discusses the pathogenesis of the prolapse of the valve.

Adult↗